Nontoxic Goiter

Updated: Oct 05, 2021
  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD  more...
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Practice Essentials

A nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not associated with abnormal thyroid function. Endemic goiter is defined as thyroid enlargement that occurs in more than 10% of a population, and sporadic goiter is a result of environmental or genetic factors that do not affect the general population.

Intrathoracic goiter causing obstruction. This pat Intrathoracic goiter causing obstruction. This patient has a visible goiter on physical examination. In addition, he has distension of his left external jugular vein, facial erythema (when compared with his shoulder), and cutaneous varicosities of venous blood draining from his head into his chest because of jugular obstruction from his goiter.

Signs and symptoms

Pertinent physical findings are limited to the evaluation of the shape, asymmetry, size, and consistency of nontoxic goiters; ultrasonographic characteristics of individual nodules within the goiter; lymphadenopathy; and assessment of thyroid function.

Examine patients with dyspnea and cough, especially with exertion, for tracheal obstruction. Note any tracheal deviation from midline.

Assess the patient’s voice for hoarseness.

See Presentation for more detail.


Laboratory studies

Assess all patients with goiter for thyroid dysfunction with a serum thyrotropin (TSH) assay. Second-generation or better TSH assays can detect clinically inapparent (subclinical) hyperthyroidism and hypothyroidism.

Imaging studies

Imaging studies used in the workup include the following:

  • Ultrasonography
  • Computed tomography (CT)
  • Magnetic resonance imaging (MRI)
  • Barium swallow

Thyroid scintigraphy is not routinely used in the assessment of goiter size unless a concern about thyroid hemiagenesis exists or the TSH level is suppressed.

See Workup for more detail.


Asymptomatic nontoxic goiters do not require treatment. Therapy is considered if growth of the entire goiter or a specific nodule is present, especially if intrathoracic extension of the goiter, compressive symptoms, or thyrotoxicosis exists. Thyroidectomy or surgical decompression provides rapid relief of obstructive symptoms. Other treatments options include radioactive iodine therapy and levothyroxine (L-thyroxine, or T4) therapy.

See Treatment and Medication for more detail.



The histopathology varies with etiology and age of the goiter. Initially, uniform follicular epithelial hyperplasia (diffuse goiter) is present, with an increase in thyroid mass. As the disorder persists, the thyroid architecture loses uniformity, with the development of areas of involution and fibrosis interspersed with areas of focal hyperplasia. This process results in multiple nodules (multinodular or adenomatous goiter). On nuclear scintigraphy, some nodules are hot, with high isotope uptake (autonomous) or cold, with low isotope uptake, compared with the normal thyroid tissue (as demonstrated in the images below).

The development of nodules correlates with the development of functional autonomy and reduction in thyroid-stimulating hormone (TSH) levels. Clinically, the natural history of a nontoxic goiter is growth, nodule production, and functional autonomy. However, abnormally high thyroid function resulting in thyrotoxicosis occurs in a minority of patients. The risk of malignancy is the same in a patient with a nodular goiter as with a solitary nodule.

See the images below.

Technetium-99m (99mTc) thyroid scan of a large, no Technetium-99m (99mTc) thyroid scan of a large, nontoxic multinodular goiter. Multiple cold and hot nodules are observed in the enlarged thyroid gland. The white arrow indicates sternal notch marker.
Areas of autonomy with excess thyroid hormone secr Areas of autonomy with excess thyroid hormone secretion in a large nodular goiter. This technetium-99m (99mTc) thyroid scan shows hot and cold nodules in a multinodular goiter. Although the patient's thyroid-stimulating hormone level had become progressively suppressed, it was within the reference range, at 0.4 mU/mL (reference range 0.35-5.5 mU/mL).


The most common worldwide cause of endemic nontoxic goiter is iodine deficiency. However, in patients with sporadic goiter, the cause is usually unknown. Nontoxic goiters have many etiologies, including the following:

  • Iodine deficiency - Goiter formation occurs with moderately deficient iodine intake of less than 50 mcg/d. Severe iodine deficiency associated with intake of less than 25 mcg/d is associated with hypothyroidism and cretinism.

  • Iodine excess - Goiter formation due to iodine excess is rare and usually occurs in the setting of preexisting autoimmune thyroid disease.

  • Goitrogens

    • Drugs - Propylthiouracil, lithium, phenylbutazone, aminoglutethimide, iodine-containing expectorants

    • Environmental agents - Phenolic and phthalate ester derivatives and resorcinol found downstream of coal and shale mines

    • Foods - Vegetables of the genus Brassica (eg, cabbage, turnips, brussels sprouts, rutabagas), seaweed, millet, cassava, and goitrin in grass and weeds

  • Dyshormonogenesis - A defect in the thyroid hormone biosynthetic pathway is inherited.

  • Childhood head and neck radiation - Radiation exposure during childhood results in benign and malignant nodules.



United States statistics

Iodine comes from ingestion of food. Iodine content of the soil determines the iodine content of plants and animals. Iodine is washed from the soil by water and is eventually washed out to the oceans. In general, areas with mountain ranges or heavy rainfall and flooding are iodine deficient. Iodine deficiency occurs in populations that depend on locally grown food and rely on vegetable protein rather than on animal or fish protein.

Studies have shown that iodine supplementation can eliminate cretinism and is highly effective in the prevention of endemic goiter. When urinary iodide falls below 25 micrograms per gram of creatinine, a palpable goiter occurs in 40-90% of the population, hypothyroidism occurs in 30-50% of the population, and cretinism occurs in 1-10% of the population. The seminal studies by David Marine, MD, in 1917 demonstrated the reduction in goiter among adolescent girls in Ohio from 20% to 5% by iodine supplementation.

Table salt has been supplemented in the United States since the 1920s for the prevention of cretinism and endemic goiter. The iodine intake in the United States, according to the National Health and Nutrition Examination Survey III (NHANES III), is adequate at 145 mcg/mg of creatinine. This adequate iodine intake in the United States eliminates the most common cause of endemic goiter in most populations.

Sporadic goiter is the most common cause of nontoxic goiter in the United States. The incidence of sporadic nontoxic goiter has been estimated in North America at approximately 5%. Sporadic goiter does not usually occur in people before puberty, and it does not have a peak incidence. Generally, the development of palpable thyroid nodules and goiter progressively increases with age. The prevalence of palpable nodules is approximately 5-6% in people aged 60 years, but on autopsy and ultrasonographic imaging findings, the incidence of small, nonpalpable nodules approaches 50% in people aged 60 years.

International statistics

More than 2.2 billion people worldwide have some form of iodine deficiency disorder. Twenty-nine percent of the world's population lives in a region that has iodine deficiency (primarily in Asia, Latin American, central Africa, and regions of Europe). Of those at risk, 655 million were known to have goiter. In the iodine-deficient regions of the world, goiter is more common than in the United States. The prevalence of goiter can be estimated based on the iodine intake of the population.

As reported by the World Health Organization (WHO), the United Nations Children's Fund (UNICEF), and the International Council for the Control of Iodine Deficiency Disorders (ICCIDD), the absence of iodine deficiency (ie, median urine iodine >100 mg/dL) is associated with a goiter prevalence of less than 5%; mild iodine deficiency (ie, median urine iodine 50-99 mg/dL), with a goiter prevalence of 5-20%; moderate iodine deficiency (ie, median urine iodine 20-49 mg/dL), with a goiter prevalence of 20-30%; and severe iodine deficiency (ie, median urine iodine 20-49 mg/dL), with a goiter prevalence of greater than 30%.

Race-, sex-, and age-related demographics

No convincing epidemiologic studies suggest that race plays an important role in the development of nontoxic goiter. Generally, the lower socioeconomic conditions in nonindustrialized countries resulting in iodine deficiency have a more important role than race does in the development of a goiter.

Diffuse and nodular goiter is more common in women than in men. According to the best estimate, the incidence of goiter in women is 1.2-4.3 times as great as that in men.

Sporadic goiter from dyshormonogenesis, a genetic error in proteins that are necessary for thyroid hormone synthesis, occurs during childhood. Endemic goiter due to iodine deficiency occurs during childhood, with the goiter's size increasing with age. Other causes of sporadic goiter rarely occur before puberty and do not have a peak age of occurrence. Thyroid nodules increase in incidence with age.



The prognosis is good. Usually, nontoxic goiters grow very slowly over many years. Any rapid growth behavior must be evaluated for either degeneration or hemorrhage of a nodule or for growth of a neoplasm.

Often, in patients who present with progressive goiter growth, those with significant dysphagia or dyspnea must be evaluated for subtotal thyroidectomy.

In some patients, radioactive iodine therapy can be considered, especially if the patient is older.

A study by Cramon et al found that both disease-specific and generic health-related quality of life discrepancies continued 6 months after treatment in benign nontoxic goiter patients. [1]

A retrospective German study found that nontoxic goiter, as well as other benign thyroid alterations, is associated with an increased risk of thyroid cancer. Half of the 2787 study participants with thyroid cancer had nontoxic goiter, compared with only one-sixth of the 2787 matched controls. [2]


Endemic goiters arising from iodine deficiency are associated with sometimes immense thyroid hypertrophy, hypothyroidism, and cretinism. Sporadic goiters are generally asymptomatic and found either by a clinician's physical examination or by the patient's observation of neck enlargement. Occasionally, the goiter may produce symptoms caused by pressure on anterior neck structures, including the trachea (wheezing, cough, globus hystericus [anterior neck pressure]), the esophagus (dysphagia), and the recurrent laryngeal nerve (hoarseness).

Rarely, the obstruction can be dangerous because of narrowing of the trachea and the development of tracheitis with edema and tracheomalacia, leading to severe narrowing of the airway with serious obstruction resulting in a respiratory emergency. (Tracheal compression and the results of its surgical treatment are seen in the images below.)

Nontoxic goiter of the thyroid gland with tracheal Nontoxic goiter of the thyroid gland with tracheal compression. An axial, noncontrast computed tomography scan through the thyroid shows significant tracheal compression.
Relief of tracheal compression after subtotal thyr Relief of tracheal compression after subtotal thyroidectomy of large, obstructive, nontoxic multinodular goiter. (A) Laryngoscopy demonstrating critical tracheal narrowing before thyroidectomy; (B) laryngoscopy showing widened patent trachea after thyroidectomy.


Complications of a nontoxic goiter occur because of growth and compression of neck structures or the development of areas of autonomy and thyrotoxicosis. [3]


Patient Education

Thyroid self-examination may be taught to patients, allowing them to monitor their own body for early changes in gland size.

For excellent patient education resources, visit eMedicineHealth's Thyroid and Metabolism Center. Also, see eMedicineHealth's patient education article Thyroid Problems.